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Background Plants memorize previous pathogen attacks and are “primed” to produce a faster and stronger defense response, which is critical for defense against pathogens. In plants, cytosines in transposons and gene bodies are reported to be frequently methylated. Demethylation of transposons can affect disease resistance by regulating the transcription of nearby genes during defense response, but the role of gene body methylation (GBM) in defense responses remains unclear. Results Here, we find that loss of the chromatin remodeler decrease in DNA methylation 1 (ddm1) synergistically enhances resistance to a biotrophic pathogen under mild chemical priming. DDM1 mediates gene body methylation at a subset of stress-responsive genes with distinct chromatin properties from conventional gene body methylated genes. Decreased gene body methylation in loss of ddm1 mutant is associated with hyperactivation of these gene body methylated genes. Knockout of glyoxysomal protein kinase 1 (gpk1), a hypomethylated gene in ddm1 loss-of-function mutant, impairs priming of defense response to pathogen infection in Arabidopsis. We also find that DDM1-mediated gene body methylation is prone to epigenetic variation among natural Arabidopsis populations, and GPK1 expression is hyperactivated in natural variants with demethylated GPK1. Conclusions Based on our collective results, we propose that DDM1-mediated GBM provides a possible regulatory axis for plants to modulate the inducibility of the immune response.

Plasticity of the root system architecture (RSA) is essential in enabling plants to cope with various environmental stresses and is mainly controlled by the phytohormone auxin. Lateral root development is a major determinant of RSA. Abiotic stresses reduce auxin signaling output, inhibiting lateral root development; however, how abiotic stress translates into a lower auxin signaling output is not fully understood. Here, we show that the nucleo-cytoplasmic distribution of the negative regulators of auxin signaling AUXIN/INDOLE-3-ACETIC ACID INDUCIBLE 12 (AUX/IAA12 or IAA12) and IAA19 determines lateral root development under various abiotic stress conditions. The cytoplasmic localization of IAA12 and IAA19 in the root elongation zone enforces auxin signaling output, allowing lateral root development. Among components of the nuclear pore complex, we show that CONSTITUTIVE EXPRESSOR OF PATHOGENESIS-RELATED GENES 5 (CPR5) selectively mediates the cytoplasmic translocation of IAA12/19. Under abiotic stress conditions, CPR5 expression is strongly decreased, resulting in the accumulation of nucleus-localized IAA12/19 in the root elongation zone and the suppression of lateral root development, which is reiterated in the cpr5 mutant. This study reveals a regulatory mechanism for auxin signaling whereby the spatial distribution of AUX/IAA regulators is critical for lateral root development, especially in fluctuating environmental conditions.

The phytohormone auxin triggers root growth inhibition within seconds via a non-transcriptional pathway. Among members of the TIR1/AFBs auxin receptor family, AFB1 has a primary role in this rapid response. However, the unique features that confer this specific function have not been identified. Here we show that the N-terminal region of AFB1, including the F-box domain and residues that contribute to auxin binding, are essential and sufficient for its specific role in the rapid response. Substitution of the N-terminal region of AFB1 with that of TIR1 disrupts its distinct cytoplasm-enriched localization and activity in rapid root growth inhibition. Importantly, the N-terminal region of AFB1 is indispensable for auxin-triggered calcium influx which is a prerequisite for rapid root growth inhibition. Furthermore, AFB1 negatively regulates lateral root formation and transcription of auxin-induced genes, suggesting that it plays an inhibitory role in canonical auxin signaling. These results suggest that AFB1 may buffer the transcriptional auxin response while it regulates rapid changes in cell growth that contribute to root gravitropism.

The political stance prediction for news articles has been widely studied to mitigate the echo chamber effect -- people fall into their thoughts and reinforce their pre-existing beliefs. The previous works for the political stance problem focus on (1) identifying political factors that could reflect the political stance of a news article and (2) capturing those factors effectively. Despite their empirical successes, they are not sufficiently justified in terms of how effective their identified factors are in the political stance prediction. Motivated by this, in this work, we conduct a user study to investigate important factors in political stance prediction, and observe that the context and tone of a news article (implicit) and external knowledge for real-world entities appearing in the article (explicit) are important in determining its political stance. Based on this observation, we propose a novel knowledge-aware approach to political stance prediction (KHAN), employing (1) hierarchical attention networks (HAN) to learn the relationships among words and sentences in three different levels and (2) knowledge encoding (KE) to incorporate external knowledge for real-world entities into the process of political stance prediction. Also, to take into account the subtle and important difference between opposite political stances, we build two independent political knowledge graphs (KG) (i.e., KG-lib and KG-con) by ourselves and learn to fuse the different political knowledge. Through extensive evaluations on three real-world datasets, we demonstrate the superiority of DASH in terms of (1) accuracy, (2) efficiency, and (3) effectiveness., Comment: 12 pages, 5 figures, 10 tables, the Web Conference 2023 (WWW)

The phytohormone auxin is a pivotal signaling molecule that functions throughout the plant lifecycle. Proper regulation of the auxin response is critical for optimizing plant growth under ever-changing environmental conditions. Recent studies have demonstrated that the signaling components that modulate auxin sensitivity and responses are functionally and mechanically diverse. In addition to auxin itself, various environmental and hormonal signals are integrated to modulate the auxin response through directly controlling auxin signaling components. This review explores the non-canonical mechanisms that modulate auxin signaling components, including transcriptional, translational, and post-translational regulation. All of these contribute to the wide range in sensitivity and complexity in auxin responses to various signaling cues.

Vascular cambium proliferation in plants is crucial for the generation of vascular tissues and for mechanical strength. Phytohormones and mobile peptides are key regulators of vascular cambial activity during secondary growth; however, the signalling cross-talk underlying their coordinated action is largely unknown. Here, we reveal that BIN2-LIKE 1 (BIL1), a glycogen synthase kinase 3, integrates the PHLOEM INTERCALATED WITH XYLEM/tracheary element differentiation inhibitory factor (TDIF) RECEPTOR (PXY/TDR) module into MONOPTEROS/AUXIN RESPONSE FACTOR 5 (MP/ARF5) transcription factor action during secondary growth. BIL1-mediated phosphorylation of MP/ARF5 enhances its negative effect on vascular cambial activity, which upregulates the negative regulators of cytokinin signalling ARABIDOPSIS RESPONSE REGULATOR 7 (ARR7) and ARR15. PXY/TDR inhibits BIL1 activity, which attenuates the effect of MP/ARF5 on ARR7 and ARR15 expression, thus increasing vascular cambial activity. Together, these results suggest that BIL1 is a key mediator that links peptide signalling with auxin–cytokinin signalling for the maintenance of cambial activity. The vascular cambium is a lateral meristem that is particularly active during secondary growth. Here, several signalling pathways (peptide, receptor, auxin and cytokinin) are linked together to explain how vascular development is regulated.

The phytohormone auxin plays crucial roles in nearly every aspect of plant growth and development. The AUXIN RESPONSE FACTOR (ARF) transcription factor family regulates auxin-responsive gene expression and exhibit nuclear localization in regions of high auxin responsiveness. Here we show that the ARF7 and ARF19 proteins accumulate in micron-sized assemblies within the cytoplasm of tissues with attenuated auxin responsiveness. We found that the intrinsically disordered middle region and the folded PB1 interaction domain of ARFs drive protein assembly formation. Mutation of a single lysine within the PB1 domain abrogates cytoplasmic assemblies, promotes ARF nuclear localization, and results in an altered transcriptome and morphological defects. Our data suggest a model in which ARF nucleo-cytoplasmic partitioning regulates auxin responsiveness, thus providing a mechanism for cellular competence for auxin signaling.

The phytohormone auxin is a key developmental signal in plants. So far, only auxin perception has been described to trigger the release of transcription factors termed Auxin Response Factors (ARFs) from their auxin/indole-3-acetic acid (AUX/IAA) repressor proteins. Here, we show that phosphorylation of ARF7 and ARF19 by BRASSINOSTEROID-insensitive2 (BIN2) can also potentiate auxin signalling output during lateral root organogenesis. BIN2-mediated phosphorylation of ARF7 and ARF19 suppresses their interaction with AUX/IAAs, and subsequently enhances the transcriptional activity to their target genes lateral organ boundaries-domain16 (LBD16) and LBD29. In this context, BIN2 is under the control of the Tracheary element differentiation inhibitory factor (TDIF)-TDIF receptor (TDR) module. TDIF-initiated TDR signalling directly acts on BIN2-mediated ARF phosphorylation, leading to the regulation of auxin signalling during lateral root development. In summary, this study delineates a TDIF-TDR-BIN2 signalling cascade that controls regulation of ARF and AUX/IAA interaction independent of auxin perception during lateral root development.